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Author Notes:

Address correspondence to this author at the Department of Pediatrics, Laval University, Québec, QC, Canada; Tel: (418) 656-4141; Fax: (418) 654-2753; E-mail: deepak.kamnasaran@crchul.ulaval.ca

We thank Dr. Kam Kamnasaran for comments on this manuscript.

The authors declare no conflict of interest.


Research Funding:

This work is supported by a Doctorate scholarship to NFA from FRSQ, and grants to DK from the CHUQ foundation, Fondation des étoiles, Canadian Foundation for Innovation, Laval University Faculty of Medicine Foundation, Natural Sciences and Engineering Research Council, and Fonds de la recherche en santé du Québec, to JH from the Canadian Institutes of Health Research, and to HCJ from the National Institutes of Health. DK is a FRSQ scholar.


  • Drug discovery
  • angiogenesis
  • microtubule
  • opioid

In-Vitro and Ex-Vivo Investigations of the Microtubule Binding Drug Targetin on Angiogenesis.


Journal Title:

Journal of pediatric oncology


Volume 1


, Pages 41-47

Type of Work:

Article | Final Publisher PDF


BACKGROUND: Intervention aimed at disrupting or inhibiting newly formed vascular network is highly desired to attenuate the progression of angiogenesis-dependent diseases. In cancer, this is tightly associated with the generation of VEGF by hypoxia inducible factor-1α following its activation by hypoxia. In light of the multiple cellular roles played by microtubules and their involvement in the processing of the hypoxia inducible factor-1α transcript, modulation of microtubule dynamics is emerging as a logical approach to suppress tumor reliance on angiogenesis. Targetin is a novel noscapinoid that interferes with microtubule dynamicity and inhibits the growth of cell lines from many types of cancers. METHODS AND RESULTS: Utilizing in-vitro and ex-vivo angiogenic models, we discovered the vascular disrupting and anti-angiogenic properties of Targetin. Targetin disrupted pre-assembled capillary-like networks of human endothelial cells by severing cell-cell junctions, inhibiting endothelial cell proliferation and metabolic activity in the presence and absence of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). Furthermore, we show that Targetin significantly inhibits the formation of neovasculature network sprouting from rat aortic explants stimulated with proangiogenic stimuli, namely VEGF or bFGF. CONCLUSION: We conclude that Targetin is a potential clinically promising anti-angiogenic agent for the treatment of many diseases including cancers.

Copyright information:

© 2013 Pharma Professional Services

This is an Open Access work distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License (http://creativecommons.org/licenses/by-nc/3.0/).

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